title: Strain-dependent cytokine profile and susceptibility to oleic acid anilide in a murine model of the toxic oil syndrome.
abstract: The toxic oil syndrome (TOS) was caused by the ingestion of an adulterated rapeseed oil containing oleic acid anilide (OAA). It was characterized by lethal symptoms in the acute phase and by symptoms of idiopathic autoimmune diseases in the chronic phase. The pathogenetic mechanisms remain unclear. In a murine model of TOS we demonstrate strain-dependent effects on the immune system after treatment with OAA intraperitoneally. While C57BL/6 (H-2b) mice develop a polyclonal B cell activation without disease symptoms, most A/J (H-2a) mice suffer an acute lethal wasting disease. These differences are reflected in the splenic cytokine gene expression and secretion and in the Ig production. Increased IgE serum levels and reduced TNF-beta mRNA suggest a Th2 cell response in C57BL/6 mice. In A/J mice, splenocytes express IL-1alpha, IL-10, and IFN-gamma mRNA in vivo and secrete high levels of TNF-alpha in vitro. These observations resemble the human condition in TOS with development of either an acute lethal disease or a chronic autoimmune-like disease. As in other chemical-induced reactions genetic susceptibility seems to be important.
authors.affiliation: Department of Dermatology, Ludwig-Maximilians-University, Frauenlobstr. 9-11, Munich, 80337, Germany.
authors.forename: C
authors.initials: C
authors.lastname: Berking
authors.forename: M V
authors.initials: MV
authors.lastname: Hobbs
authors.forename: R
authors.initials: R
authors.lastname: Chatelain
authors.forename: M
authors.initials: M
authors.lastname: Meurer
authors.forename: S A
authors.initials: SA
authors.lastname: Bell
mesh_terms: D000813:Anilides / Q000506:poisoning*; D000818:Animals; D001327:Autoimmune Diseases / Q000139:chemically induced* / Q000235:genetics / Q000276:immunology; D002478:Cells, Cultured; D016207:Cytokines / Q000096:biosynthesis*; D004249:DNA Damage; D004195:Disease Models, Animal; D004198:Disease Susceptibility; D005260:Female; D007073:Immunoglobulin E / Q000097:blood*; D007371:Interferon-gamma / Q000096:biosynthesis / Q000235:genetics; D007375:Interleukin-1 / Q000096:biosynthesis / Q000235:genetics; D016753:Interleukin-10 / Q000096:biosynthesis / Q000235:genetics; D008233:Lymphotoxin-alpha / Q000096:biosynthesis / Q000235:genetics; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D009829:Oleic Acids / Q000506:poisoning*; D010938:Plant Oils / Q000506:poisoning; D012333:RNA, Messenger / Q000032:analysis; D013154:Spleen / Q000276:immunology; D013163:Splenomegaly / Q000139:chemically induced / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000235:genetics; D019282:Wasting Syndrome / Q000139:chemically induced* / Q000235:genetics / Q000276:immunology
chemical_list: D000813:Anilides; D016207:Cytokines; D007375:Interleukin-1; D008233:Lymphotoxin-alpha; D009829:Oleic Acids; D010938:Plant Oils; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D007073:Immunoglobulin E; C038731:oleoylanilide; D007371:Interferon-gamma